A5068744182- Congenital heart defects research
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Mitochondrial Function and Pathology
- Genetics and Neurodevelopmental Disorders
- Neural dynamics and brain function
- Neuroinflammation and Neurodegeneration Mechanisms
- RNA modifications and cancer
- Ion channel regulation and function
- RNA Research and Splicing
- Cardiac Fibrosis and Remodeling
- Genetic factors in colorectal cancer
St. Jude Children's Research Hospital
2016-2017
University of California, Riverside
2013
Hemizygous deletion of a 1.5- to 3-megabase region on chromosome 22 causes 22q11.2 syndrome (22q11DS), which constitutes one the strongest genetic risks for schizophrenia. Mouse models 22q11DS have abnormal short-term synaptic plasticity that contributes working-memory deficiencies similar those in We screened mutant mice carrying hemizygous deletions genes and identified haploinsufficiency Mrpl40 (mitochondrial large ribosomal subunit protein 40) as contributor potentiation (STP), major...
One of the most important functions astrocytes is removal glutamate released during synaptic transmission. Surprisingly, mechanisms by which astrocyte uptake acutely modulated remain to be clarified. Astrocytes express metabotropic receptors (mGluRs) and other G protein-coupled (GPCRs), are activated neuronal activity. Here, we test hypothesis that astrocytic group I mGluRs regulate in situ. This was tested acute mouse hippocampal slices. Activation mGluRs, using a tetanic high-frequency...
Abstract A feature in patients with constitutional DNA-mismatch repair deficiency is agenesis of the corpus callosum, cause which has not been established. Here we report a previously unrecognized consequence MSH2, protein known primarily for its function correcting nucleotide mismatches or insertions and deletions duplex DNA caused by errors replication recombination. We documented that Msh2 causes dysmyelination axonal projections callosum. Evoked action potentials myelinated callosum...